Ali Yaghi. Yaseen Fatayer. M.Khatatbeh

Transcription

1 6 Ali Yaghi Yaseen Fatayer M.Khatatbeh P a g e 1

2 pancreatic secretions note: The pancreas has endocrine (secretions are released toward the blood) and exocrine(secretions are released through the canalicular system to the interstitial fluid) functions. In pancreas, there are acinar cells and duct cells (in the exocrine system). The acinar cells release enzymes, and the duct cells release water and electrolytes(same as salivary glands). The secretions of the pancreas are released through a duct. This duct unites with another duct that is coming from the liver forming hepatopancreatic duct. The hepatopancreatic duct has an opening called Oddi sphincter. Anatomical view to the Oddi sphincter : we have a sphincter which is guarding this opening which is important to prevent the reflux from the pancreatic enzymes to the pancreas again. Histological view: the cells that secrete enzymes have vesicles, but duct cells don't have vesicles. Pancreatic enzymes(proteolytic enzymes): 1- Trypsin(ogen) 2- Chemotrepsin(ogen) 3- (Pro)Carboxypeptidase Note: All of these are endopeptidases (cut from the middle) except carboxypeptidase which is an exopeptidase (cuts on c end). Note: All these enzymes are released as proenzymes (inactive), and the activation occurs in the duodenum. At the duodenum, we have the enzyme enterokinase which is responsible for converting trypsinogen into trypsin (activating it by phosphorylation),and the Trypsin activates others by cutting them(endopeptidase). P a g e 2

3 Note: Pancreatic enzymes aren't released as active enzymes to protect the pancreas from eating it self Note: (oddi sphincter) prevents the reflux of pancreatic secretions and protects the pancreas. Therefore, alcoholics suffer from acute pancreatitis because of the relaxation of the sphincter and the reflux. Carbs digesting enzymes amylase: secreted as active enzyme to convert Starch (polysaccharide) into disaccharides. Lipolytic enzymes: 1- lipases 2- phospholypases 3- cholesterol ester hydroxylase Note: secreted as active and inactive enzymes. water and electrolytes secretion *Duct cells secrete water and electrolytes( the mechanism same as in stomach) *We are forming the bicarbonate in duct cells and secreting it toward the lumen and absorbing H+ ions. *At low secretion level: low bicarbonate content and high Cl-.At higher levels we have higher bicarbonate content (that means you formed more bicarbonate upon stimulating ) P a g e 3

4 *The absorbing of Cl- is according to the potentials, once you have more releasing of bicarbonate, you are reducing the release of the other ions. Controlling of pancreatic secretions: 1- Neural control. 2- Hormonal control. ** Neural control (autonomic nervous system, and some enteric fibers) Parasympathetic: activation by vagal stimulation enteric nervous system release of Ach, VIP, and GRP (Gastrin releasing protein). Sympathetic: indirect inhibition via vasoconstriction Hormonal control: 1- Secretin: it is secreted from the duodenal mucosa, and it effects duct cells (increase water and HCO3- secretion) 2- Cholicyctokinin : it affects the acinar cells(enzyme secretion).acinar cells have receptors for CCK (CCK-A receptor), and it causes increase of the enzymatic secretions. CCK also increases the vagovagal reflexes. P a g e 4

5 vagovagal: vagal nerve has sensory fibers and efferent fibers (increases parasympathetic and stimulate enzyme secretion) Note: this is an example proves that endocrine cells can act on the neurons and change its activity. 3- Pancreatic polypeptide: it inhibits the pancreatic activity by: *Inhibiting Ach release from enteric nervous system. *Inhibiting vagal output of the CNS. Control of pancreatic secretion (summary): - Cephalic phase (activation) - Gastric phase (activation) - Intestinal phase (activation) - No phase ( inhibiting) (more pancreatic polypeptide in no phase). Liver secretions *we will concentrate on Excretion of cholesterol and bilirubin. P a g e 5

6 *Bilirubin is waste material from hemoglobin, low secretion =high bilirubin= jaundice. Note: In order to excrete bilirubin, it must be conjugated with (glucoronide, sulfate, other substances) to make it more soluble and hydrophilic. Hepatic lobule- blood and bile paths The liver has hepatic lobules (hexagonal structure composed of hepatic cells), at every angle of the 6 angles, there is a branch of the portal vein (the vein that transmits the blood from the intestines to the liver). At the center of the hebatic lobe, there is a vein called central vein. The blood circulates between the hepatic cells starting from the portal vein to the central vein. There is a canal in the hepatic lobules that secretes the bile, this canal is called bile canal, and bile is flowing from the center to the prephery. each hepatocyte is having 2 poles, one is facing these sinosoids (bigger than capillary) and the other pole is facing the bile duct. P a g e 6

7 bile salts They are synthesized from cholesterol.cholesterol is transformed to bile acid (cholic acid and chenodeoxycholic acid), and these 2 are conjugated to glycine or taurine to synthesise bile salts (more hydrosoluble). How do the bile salts go to gall bladder? By the relaxation of the gall bladder, the pressure inside it is lower than in the duct, so the bile moves from the bile duct to the gall bladder and get stored in it (some absorption of water and electrolytes takes place ). Once a meal is ingested, the bile salts are secreted from the gall bladder to the duodenum by the contraction of the bladder. Note: By comparing of bile from the liver directly, and the one from the gall bladder, we find that bile salts are more concentrated in the gall bladder bile. Note: if someone has done gall bladderictomy, this person must reduce his fat intake (must not eat fat rich meals because its bile is less efficient than in normal people). Gall bladder stones: hypomotility of gall bladder leads to more reabsorbtion of water and electrolytes from the bile, so it is less soluble, and that what makes the gall bladder stones. Notes: 1- Hypomotility of gall bladder is caused by deformity or inflammation. 2- stones might cause inflammation. Bile salts reabsorbtion: *80 percent of bile salts are reabsorbed by the enterohepatic circulation, and then reusing it again. *The 20 percent lost can be compensated by de novo synthesis from cholesterol. P a g e 7

8 Modification of bile salts in the intestine to secondary bile acid: Cholic acid deoxycholic acid. Chenodeoxycholic acid lithocholic acid Note: the non modified bile salts can be reabsorbed unlike the modified (secondary bile acids) Control of hepatic secretions: In addition to the autonomic nervous system (contraction of the gall bladder and the release of the bile salts) 1- CCK: Its main activity is to stimulate contraction of the gall bladder, which is stimulated by the eating of fat content chyme. 2- Secretin: works over duct cells to increase water and electrolytes 3- Somatostatin: inhibitory for duct cells. digestion and absorbtion: esophagus: no absorption small intestine: specialized organ for absorption and digestion colon: highly reabsorption of fluids from the feces. small intestine: the mucosa is folded which increases the surface area 3 times. over these folds we have villi (papillary like structure, highly capillariesed, also there is lymphatic vessels which are called central lacteals_ which has importance for absorbing some materials) with these villi, we increase the surface area 10 times, (3 times is from the folds) we have cells which are lining the villi, the luminal membrane of these cells is also folded, forming microvilli (brush border), over the brush boarder we have some enzymes, like enterokinase. The overall increase of the surface area of the small intestine is 600 times. P a g e 8

9 1cm of the intestine is equal to 600cm (functionally) P a g e 9